| dc.creator | Ferrero, Maximiliano Ruben | |
| dc.creator | Tavares, Luciana Pádua | |
| dc.creator | Garcia, Cristiana Couto | |
| dc.date | 2022-05-09T21:01:33Z | |
| dc.date | 2022-05-09T21:01:33Z | |
| dc.date | 2022 | |
| dc.date.accessioned | 2023-09-26T20:16:51Z | |
| dc.date.available | 2023-09-26T20:16:51Z | |
| dc.identifier | FERRERO, Maximiliano Ruben; TAVARES, Luciana Pádua; GARCIA, Cristina Couto. The Dual Role of CCR5 in the Course of Influenza Infection: Exploring Treatment Opportunities. Frontiers in Immunology, v. 12, Article 826621, p. 1 - 8, Jan. 2022. | |
| dc.identifier | 1664-3224 | |
| dc.identifier | https://www.arca.fiocruz.br/handle/icict/52594 | |
| dc.identifier | 10.3389/fimmu.2021.826621 | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/8853206 | |
| dc.description | Influenza is one of the most relevant respiratory viruses to human health causing annual
epidemics, and recurrent pandemics. Influenza disease is principally associated with
inappropriate activation of the immune response. Chemokine receptor 5 (CCR5) and its
cognate chemokines CCL3, CCL4 and CCL5 are rapidly induced upon influenza infection,
contributing to leukocyte recruitment into the airways and a consequent effective antiviral
response. Here we discuss the existing evidence for CCR5 role in the host immune
responses to influenza virus. Complete absence of CCR5 in mice revealed the receptor’s
role in coping with influenza via the recruitment of early memory CD8+ T cells, B cell
activation and later recruitment of activated CD4+ T cells. Moreover, CCR5 contributes to
inflammatory resolution by enhancing alveolar macrophages survival and reprogramming
macrophages to pro-resolving phenotypes. In contrast, CCR5 activation is associated
with excessive recruitment of neutrophils, inflammatory monocytes, and NK cells in
models of severe influenza pneumonia. The available data suggests that, while CCL5
can play a protective role in influenza infection, CCL3 may contribute to an overwhelming
inflammatory process that can harm the lung tissue. In humans, the gene encoding CCR5
might contain a 32-base pair deletion, resulting in a truncated protein. While discordant
data in literature regarding this CCR5 mutation and influenza severity, the association of
CCR5delta32 and HIV resistance fostered the development of different CCR5 inhibitors,
now being tested in lung inflammation therapy. The potential use of CCR5 inhibitors to
modulate the inflammatory response in severe human influenza infections is to
be addressed. | |
| dc.format | application/pdf | |
| dc.language | eng | |
| dc.publisher | Frontiers Media | |
| dc.rights | open access | |
| dc.subject | Gripe | |
| dc.subject | Receptor de quimiocina 5 | |
| dc.subject | CCR5delta32 | |
| dc.subject | CCR5 | |
| dc.subject | CCL3 | |
| dc.subject | Influenza | |
| dc.subject | Chemokine receptor 5 | |
| dc.subject | CCR5delta32 | |
| dc.subject | CCR5 | |
| dc.subject | CCL3 | |
| dc.title | The Dual Role of CCR5 in the Course of Influenza Infection: Exploring Treatment Opportunities | |
| dc.type | Article | |
